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首页> 外文期刊>American Journal of Physiology >Sex differences in maternal gestational hypertension-induced sensitization of angiotensin II hypertension in rat offspring: the protective effect of estrogen
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Sex differences in maternal gestational hypertension-induced sensitization of angiotensin II hypertension in rat offspring: the protective effect of estrogen

机译：大鼠后代血管紧张素II高血压诱导孕妇妊娠高血压诱导的性差异：雌激素的保护作用

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Recent studies demonstrate that maternal hypertension during pregnancy sensitizes an angiotensin (ANG) II-induced increase in blood pressure (BP) in adult male offspring that was associated with upregulation of mRNA expression of several renin-angiotensin-aldosterone system (RAAS) components and NADPH oxidase in the lamina terminalis (LT) and paraventricular nucleus (PVN). The purpose of the present study was to test whether there are sex differences in the maternal hypertension-induced sensitization of ANG II hypertension, and whether sex hormones are involved in the sensitization process. Male offspring of hypertensive dams showed an enhanced hypertensive response to systemic ANG II when compared with male offspring of normoten-sive dams and to female offspring of either normotensive or hypertensive dams. Castration did not alter the hypertensive response to ANG II in male offspring. Intact female offspring had no upregulation of RAAS components and NADPH oxidase in the LT and PVN, whereas ovariectomy (OVX) upregulated mRNA expression of several RAAS components and NADPH oxidase in these nuclei and induced a greater increase in the pressor response to ANG II in female offspring of hypertensive dams compared with female offspring of normotensive dams. This enhanced increase in BP was partially attenuated by 17β-estradiol replacement in the OVX offspring of hypertensive dams. The results suggest that maternal hypertension induces a sex-specific sensitization of ANG II-induced hypertension and mRNA expression of brain RAAS and NADPH oxidase in offspring. Female offspring are protected from maternal hypertension-induced sensitization of ANG II hypertension, and female sex hormones are partially responsible for this protective effect.
机译：最近的研究表明，妊娠期间的母体高血压致敏成年男性后代血压（BP）的血管素（Ang）II诱导的血压增加，这与MRNA血管紧张素体系（RAAS）组分和NADPH的mRNA表达相关联氧化酶在薄层端子（LT）和椎间露核（PVN）中。本研究的目的是测试母体高压诱导的Ang II高血压致敏是否存在性别差异，以及性激素是否参与敏化过程。高血压大坝的男性后代对系统ang II的高血压反应显示，与正常的稳压水坝的男性后代相比，以及正常衰退或高血压坝的女性后代。阉割在男性后代没有改变对Ang II的高血压反应。完整的雌性后代在LT和PVN中没有对RAAs组分和NADPH氧化酶的上调，而卵巢切除术（OVX）在这些核中的几种RAAs组分和NADPH氧化酶的上调MRNA表达，并且在雌性中诱导了对ang II的压力响应越大增加高血压水坝的后代与正规水坝女性后代相比。通过高血压坝OVX后代的17β-雌二醇替代，这种增强的BP增强的增加部分衰减。结果表明，孕产妇高血压诱导了异常诱导的Ang II诱导的高血压和mRNA表达在后代脑Raas和NADPH氧化酶的性别特异性敏化。女性后代受到母体高压诱导的致敏致敏Ang II高血压，并且女性性激素部分负责这种保护作用。

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